The specific aim of the proposed study is to investigate rational means of ameliorating injury to the ischemic myocardium that accrues during prolonged coronary flow deprivation associated with aortic cross clamping during open heart surgery. A bloodless flaccid, non-beating heart at normothermic temperature facilitates the repair of various cardiac defects. Amelioration will be attempted through: (1) avoidance of energy depleting ischemic arrest by alternative arrest procedures; (2) pharmacologic prophylaxis to (a) decrease nucleoside efflux, (b) to block hypermetabolism and hyperfunction and (c) to prevent platelet-platelet adhesion and emboli formation. Restorative measures will be attempted through: (1) postischemic treatment to increase recovery rate; (2) removal of potentially toxic metabolites; and (3) administration of hypertonic substances. The ultimate objective of this project is to devise a means of safely extending the time of normothermic cardiac arrest (greater than 30 to 45 minutes) so that complicated operative procedures may be performed with technical ease. In addition, it is hoped that a non-invasive device or metabolic probe may be constructed that will allow the surgeon to continuously evaluate and monitor the extent of metabolic dysfunction during the cross-clamp period. BIBLIOGRAPHIC REFERENCES: Rao, K.S., Schutz, R., Feinberg, H. and Levitsky, S.: Metabolic evidence that regional hypothermia induced by cold saline protects the heart during ischemic arrest. Jour. Surg. Res. 20:421, 1976. Rao, K.S., Levitsky, S., Holland, C., Feinberg, H., Fialkowski, W. and Merchant, F.: Does Potassium Chloride Induced Cardiac Arrest Protect the Myocardium during aortic cross clamping? Surgical Forum 27:262, 1976.